The control of motor behavior by the striatum involves the action of a variety of neurotransmitters, including glutamate and dopamine (afferents to the striatum), acetylcholine and GABA (interneurons) and GABA, substance P and possibly adenosine (efferents). To better understand control of GABAergic function we examined the effects on GABA turnover of injection into rat striatum of several agonists and antagonists of these transmitters. As an index of turnover, we injected gabaculine (an inhibitor of GABA synthesis) directly into the striatum, and measured the rate of GABA accumulation. Injection of excitatory amino acids (glutamate and kainic acid) increased GABA turnover. Injection of a glutamate antagonist (glutamate di-ethyl ester) produced the opposite effect, and blocked the action of glutamate. Local injection of a dopamine agonist also increased GABA accumulation. Cholinergic agonists (carbachol and oxotremorine) had no effect on GABA accumulation.